Don’t smoke to fast or to slow. But just right!

IMG_0615

When smoking cannabis, how a person inhales is a significant contributor to the amount of the desired cannabinoid that enters the bloodstream. Bioavailability is the amount of an administered drug that is absorbed by the body. It is the consensus that the bioavailability of cannabis when inhaled is approximately 25%; where the bioavailability of ingested cannabis is 6% (more on increasing the bioavailability of edibles in a later blog). Through controlled experiment, scientists discovered six variables affecting the availability of smoked cannabis:

Smoking dynamics (most significant)

Smoking dynamics is the method, and biological mechanics of an individual’s inhalation while smoking.

  • Puff volume is a part of smoking dynamics; it is the number of inhalations a person takes from a joint. In a study examining blood THC levels in cannabis smokers, researchers discovered, puff volume affects the amount of THC available in the bloodstream.
    • Reduced puffs per minute will increase the time it takes to reach peak THC blood levels. Additionally, slower puff volume increases the time it takes for the body to return to baseline after smoking. However, THC does not reach the same peak plasma levels compared to increased puff volume.
    • Peak THC blood plasma levels are higher with increased puff volume. Also, peak THC levels are achieved early in the smoking session compared to a lower volume. Nevertheless, the body returns to baseline significantly faster with increase puff volume once smoking stops.

The smoking dynamic of a water-pipe is similar to accelerated puff volume of a joint.

Generally, THC plasma concentrations increased progressively for as long as puffs were taken. As a result, peak THC concentrations does not occur until the end of the smoking session. Finding suggests that increased volume of smoke (approximately 200 ml) every 2.5 minutes delivers adequate THC to the blood to balance the drug’s rate of disappearance into the extravascular compartment.

Cannabinoid potency

A higher percentage of the cannabinoid desired increases the amount of the cannabinoid in the bloodstream.

 Amount of cannabinoid left after pyrolytic destruction

Pyrolytic destruction is the decomposition brought about by high temperatures. Pyrolysis destroys a portion of cannabinoid desired when smoking cannabis. Researchers found 20% to 30% of THC is lost to pyrolysis when smoking from a joint or water-pipe.

Amount of cannabis lost in the side-stream smoke

When a person smokes a joint, smoke produced is either inhaled when puffs are taking (main-stream) or escapes to the surrounding environment (side-stream). Initial findings studying the amount of THC lost in side-stream concluded 40%-50% of THC is lost. However, researchers may have overestimated these findings. The study used a two puff per minute protocol. Others have commented that most individuals take more than two puffs per minute. Nevertheless, THC lost to side-stream while smoking a joint increase the more it is idle. Researchers noted that 90% of the total smoke time is idle; therefore, a significant amount of THC still escapes through side-stream.

 Method used (joint or water-pipe)

Water-pipe

  • ~20% lost in bowl residue
  • ~8% lost in stem and pipe residue
  • ~3.5% product lost in water from pipe
  • ~8% lost in plant material from water
  • ~40% main-stream smoke (usable product)

Joint

  • up-to 40-50% lost to side-stream (if
  • 20 to 30% lost to pyrolytic destruction
  • 20 to 30% In mainstream smoke (usable product)

Note: No side-stream was reported for the water-pipe because the protocol used only enough cannabis for one complete inhalation (hit).

Amount of marijuana trapped in the mucosa of the upper respiratory tract

While smoking cannabis, the upper respiratory tract traps a small amount of THC in the mucosa thereby reducing bioavailability. Studies found the amounts of THC lost is considered of minor importance.

In closing, despite the listed variables above, there are still reports of wide fluctuations in the bioavailability of cannabis among individuals. Variations in bioavailability are because of unique biological differences people have between each other. Biological uniqueness means a significant amount of people can either feel the effects of cannabis at lower doses or may need higher doses to feel any effect. If a person is new to cannabis, it will benefit them to start with decrease potency and increase potency if required. Additionally, individuals can also increase puff volume to increase the availability of the desired cannabinoid. Following these procedures will reduce the incidents of a temporary psychotic episode from a significant one-time dose when using cannabis.

References

Marijuana smoking: Factors that influence the bioavailability of tetrahydrocannabinol. (1990). In N. C. Chiang, & R. L. Hawks (Eds.), Research findings on smoking of abused substances (pp. 42-62). Rockville, Maryland: National Institute on Drug Abuse.

Cannabinoid Hyperemesis Syndrome

IMG_0881Cannabinoid hyperemesis syndrome (CHS) is said to be brought on by chronic heavy use of cannabis. Symptoms include recurrent episodes of nausea, vomiting, and abdominal pain. Sufferers of CHS can find temporary relief of symptoms by taking either a hot bath or shower. Case studies show that CHS resolves itself when cannabis use stops. CHS often gets misdiagnosed and can lead to costly ineffective treatments. A recent study examining the prevalence of CHS in urban cannabis smokers estimate that between 2.13 to 3.38 million may suffer symptoms similar to CHS. All cases seem to come from excessive smoking of cannabis and not edibles.

The author of this post would like to see more studies examining the nutritional choices and physical activity levels of individuals suffering from cannabinoid hyperemesis syndrome. Nutrition and physical activity are modifiable risk factors that can resolve a multitude of health issues. It would not be a big surprise if exercise and proper diet would reduce CHS symptoms. Nevertheless, futures studies will hold the answers.

References

Habboushe, J., Rubin, A., Liu, H., & Hoffman, R. S.The prevalence of cannabinoid hyperemesis syndrome among regular marijuana smokers in an urban public hospital. Basic & Clinical Pharmacology & Toxicology, , n/a-n/a. doi:10.1111/bcpt.12962

Sullivan, S. (2009). Cannabinoid hyperemesis. Canadian Journal of Gastroenterology, 24(5), 284-285. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886568/

Cannabis and Psychosis

IMG_1594

 

The prevalence of any population having a psychotic disorder is approximately 3.5%; additionally, the incidence of schizophrenia is ~1%.  Just as there are an infinite number studies on ways predicting psychotic disorders, there are an equal amount of studies attempting to reduce the number of cases among the population. Nevertheless, without any background in research methods, one may not know what to make of all these studies.

Before we start, the following is a fundamental review of some research methods used in science.

A longitudinal study is a study looking at a group of participants over a period. Longitudinal studies are good at identifying changes in a system over time. However, they are not good at establishing causation.

Experimental research another conventional method used in science establishes cause and effect. Unfortunately, many restrictions on cannabis prohibit most experimental studies on humans.

A meta-analysis is a form of research synthesis that takes a group of studies and uses statistics to increase the power of an outcome. One-way researchers use a meta-analysis is to increase the likely hood that a variable is affecting a change. A meta-analysis is only as good as the studies used in the analysis. Note, if studies examined in a meta-analysis are from longitudinal research, the reader should not disregard information when experimental research is missing. However, the reader should realize these shortfalls and take into consideration that there may be more than the examined variable affecting the outcome.

Tetrahydrocannabinol (THC) is the psychoactive component of cannabis. Significant one-time doses of THC can produce a temporary mild psychotic episode in healthy naive cannabis users. Very little is known about THC increasing the prevalence of psychotic disorders in the cannabis population. This article reviews recent finding involving cannabis and psychosis.

A widely cited meta-analysis found that regular cannabis users may have a two-fold increase in psychosis. Another analysis examining the early onset of psychosis found adolescent cannabis use increased the risk of psychosis late in life. However, the method of analysis from both studies consisted of longitudinal and population-based all of which does not establish causation. Moreover, the studies used did not set a starting point for comparisons. Without a baseline, researchers cannot ascertain if an individual with psychosis is attracted to cannabis use or does cannabis use increase the risk of psychosis.

People do not need cannabis to develop psychosis. However, cannabis may add to the development of psychosis in at-risk individuals. A journal article from the Current Opinion in Psychiatry revealed that adolescent and adults already at risk of psychosis increase their risk when using cannabis.

That does not mean cannabis does not benefit individuals diagnosed with psychosis or schizophrenia. In another meta-analysis, researchers observed that people diagnosed with schizophrenia who use cannabis function better cognitively than individuals with schizophrenia that do not use cannabis. The at-risk population should consult proper medical professionals about the hazards cannabis may contribute to their mental health and seek information on the proper use of cannabis.

The cannabinoid Cannabidiol (CBD) is known to counter the psychoactive effect of cannabis. Additionally, scientist found CBD to have the same effect and a superior safety profile compared to the standard ant-psychotic medication. Therefore, CBD may reduce psychotic episodes and may soon be a safe alternative to aggressive antipsychotic medication after more studies.

In closing, cannabis use may increase the risk of psychosis and schizophrenia by two-fold in the cannabis population. Meaning the risk of a psychotic disorder may increase from 3.50% to 7% or from 1% to 2% in schizophrenia. Nevertheless, researchers will need more experimental studies to prove further how cannabis affects psychosis.

Although cannabis increases the risk of psychosis in the at-risk population, when correctly used, cannabis improved cognition in people with schizophrenia. At-risk individuals should seek professional medical advice before starting cannabis.

CBD is shown to counter the psychoactive effect of THC. Recently CDB presented an improved safety profile compared to the standard ant-psychotic medication suggesting CBD may be a safer alternative. More studies will be needed using CBD as an alternative to conventional medication.

Lastly, cannabis is not as dangerous as many perceive, and it is not as safe as others argue; the truth will be found somewhere in the middle.

References

Bhattacharyya, S., Morrison, P. D., Fusar-Poli, P., Martin-Santos, R., Borgwardt, S., Winton-Brown, T., . . . McGuire, P. K. (2009). Opposite effects of Δ-9-tetrahydrocannabinol and cannabidiol on human brain function and psychopathology. Neuropsychopharmacology, 35, 764. Retrieved from http://dx.doi.org/10.1038/npp.2009.184

Di Forti, M., Morrison, P. D., Butt, A., & Murray, R. M. (2007). Cannabis use and psychiatric and cogitive disorders: The chicken or the egg? Current Opinion in Psychiatry, 20(3) Retrieved from https://journals.lww.com/co-psychiatry/Fulltext/2007/05000/Cannabis_use_and_psychiatric_and_cogitive.10.aspx

D’Souza, D. C., Perry, E., MacDougall, L., Ammerman, Y., Cooper, T., Wu, Y., . . . Krystal, J. H. (2004). The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: Implications for psychosis.Neuropsychopharmacology, 29, 1558. Retrieved from http://dx.doi.org/10.1038/sj.npp.1300496

Large, M., Sharma, S., Compton, M. T., Slade, T., & Nielssen, O. (2011). Cannabis use and earlier onset of psychosis: A systematic meta-analysis. Archives of General Psychiatry, 68(6), 555-561. Retrieved from http://dx.doi.org/10.1001/archgenpsychiatry.2011.5

Leweke, F. M., Piomelli, D., Pahlisch, F., Muhl, D., Gerth, C. W., Hoyer, C., . . . Koethe, D. (2012). Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Translational Psychiatry, 2, e94. Retrieved from http://dx.doi.org/10.1038/tp.2012.15

Moore, T. H. M., Zammit, S., Lingford-Hughes, A., Barnes, T. R. E., Jones, P. B., Burke, M., & Lewis, G.Cannabis use and risk of psychotic or affective mental health outcomes: A systematic review. The Lancet, 370(9584), 319-328. doi:10.1016/S0140-6736(07)61162-3

Perala , J., Suvisaari, J., Saarni, S. I., & al, e. (2007). Lifetime prevalence of psychotic and bipolar i disorders in a general population. Archives of General Psychiatry, 64(1), 19-28. Retrieved from http://dx.doi.org/10.1001/archpsyc.64.1.19

Yucel, M., Bora, E., Lubman, D. I., Solowij, N., Brewer, W. J., Cotton, S. M., . . . Pantelis, C. (2012). The impact of cannabis use on cognitive functioning in patients with schizophrenia: A meta-analysis of existing findings and new data in a first-episode sample. Schizophrenia Bulletin, 38(2), 316-330. Retrieved from http://dx.doi.org/10.1093/schbul/sbq079

Cannabis and Memory

IMG_0758

Many people hear urban legends about the damage that cannabis can do to memory. Most if not all of the myths lack evidence-based research. Additionally, if the tale was from a study, it was cited incorrectly, or the storyteller had a personal bias. This post explores the recent studies involving memory impairment and cannabis.

Thus far evidence points to cannabis temporarily impairing both short-term memory and the ability to make long-term memories from short-term. The experience of memory impairment happens when an acute dose is taking at once or during prolonged exposure. Nevertheless, cannabis does not reduce the ability to recall information once a memory is in long-term storage.

Reductions in attention and short-term working memory function are debatable cognitive impairments associated with cannabis. Both are said to have similar handicaps as short-term memory. Still, they are controversial because of the method of analysis. When running a meta-analysis with a large group of studies, one team of researchers found no causation of cannabis affecting attention or working memory. However, a second team rerunning the analysis with fewer studies found temporary cognitive impairments. Nevertheless, researchers found that the absence of cannabis for approximately 30 days (one month), eliminated any previous cognitive limitations. At a follow-up test of cognition, past cannabis users tested the same as non-cannabis users. Meaning when a person decides to suspend cannabis there may be no lasting cognitive impairments.

One of many cannabinoids is tetrahydrocannabinol (THC); THC is the psychoactive component of cannabis; it is the primary causal agent in temporary memory impairment when using Cannabis. Another cannabinoid Cannabidiol (CBD) whose medical value is still in the infancy of research is antagonistic to many of THC’s impairing effects. CBD reduces the psychoactive effect and cognitive impairments of THC. Thus, taking CBD with THC may counteract any acute and long-term cognitive impairments when using cannabis.

In closing, data shows THC a cannabinoid in cannabis effect short-term memory and diminishes the ability to store short-term memory in long-term storage. However, long-term memory recall is not affected by cannabis use. Cannabis may or may not affect attention and short-term working memory. Suspending use for one month stopped any cognitive impairments associated with cannabis. Lastly, CBD may hinder any acute and long-term cognitive impairments when using cannabis.

References

Broyd, S. J., van Hell, H. H., Beale, C., Yücel, M., & Solowij, N. (2016). Acute and chronic effects of cannabinoids on human Cognition—A systematic review. Biological Psychiatry, 79(7), 557-567.

GRANT, I., GONZALEZ, R., CAREY, C. L., NATARAJAN, L., & WOLFSON, T. (2003). Non-acute (residual) neurocognitive effects of cannabis use: A meta-analytic study. Journal of the International Neuropsychological Society, 9(5), 679-689.

Morgan, C. J. A., Schafer, G., Freeman, T. P., & Curran, H. V. (2010). Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: Naturalistic study. The British Journal of Psychiatry, 197(4), 285-290.

Nadia Solowij, R. B. (2008). The chronic effects of cannabis on memory in humans: A review. Current Drug Abuse Reviews, 1(1)

Schreiner, A. M., & Dunn, M. E. (2012). Residual effects of cannabis use on neurocognitive performance after prolonged abstinence: A meta-analysis. Experimental and Clinical Psychopharmacology, 20(5), 420-429.

Volkow ND, Swanson JM, Evins AE, DeLisi LE, Meier MH, Gonzalez R, Bloomfield MAP, Curran HV, Baler R. (2016). Effects of cannabis use on human behavior, including cognition, motivation, and psychosis: A review. JAMA Psychiatry, 73(3), 292-297.